APOPTOSIS AND VASCULAR WALL REMODELING IN HYPERTENSION

Vascular structure plays a key role in the pathogenesis of hypertensio n. Because it is less readily reversible than protein accumulation, DN A accumulation in the arterial wall may be considered as a record of p ast episodes of vascular growth, contributing to the persistence of th e vascular disease. Apoptosis, a ubiquitous and highly regulated form of programmed cell death that is involved in tissue morphogenesis and homeostasis as the essential counterpart of cell replication, is poten tially involved in the regulation of vascular structure, via the delet ion of cells in the vessel wall. We discuss how the current knowledge on apoptosis may provide insights into the pathogenesis of vascular wa ll remodeling, with an emphasis on the biology of vascular smooth musc le cells. Evidence suggests that heightened cell replication rates are often associated with increased apoptosis, as for smooth muscle cells in genetic hypertension or in arterial repair after injury. However, apoptotic cell death may also be regulated independently of cell growt h. The triggering of apoptosis depends on a balance of environmental c ues that are not specific to apoptosis. However, there is a common set of key biochemical events mediating apoptosis (i.e., committing the c ell to die), thus providing a basis for the design of novel pharmacolo gical strategies specifically targeting apoptotic cell death. The iden tification of biochemical markers of apoptosis and other methodologica l advances will ultimately help in understanding the role of apoptotic cell death in vascular remodeling and hypertensive end-organ damage.